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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
1992-11-18
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pubmed:abstractText |
T cell activation is dependent upon calcium influx and protein kinase C activation, with subsequent lymphocyte proliferation dependent upon IL-2. Abnormalities in T cell proliferation, including abnormal calcium influx and defective protein kinase C activation, have been identified in aged mice and humans and many autoimmune diseases including diabetes, lupus and scleroderma. Since UCD line 200 chickens, which spontaneously develop a scleroderma-like disease, have both thymic defects and a diminished peripheral blood lymphocyte response to IL-2, we have further investigated T cell function in these birds. Interestingly, line 200 T cells respond poorly in vitro to a variety of diversely acting T cell mitogens including concanavalin A, phytohemagglutinin and anti-chicken CD3 monoclonal antibody. Moreover, they do not respond well even to phorbol myristate acetate in conjunction with ionomycin. Addition of exogenous IL-2-containing supernatant concurrently with mitogenic stimulation also had no significant effect. Analysis of intracellular free calcium demonstrated that the lymphocytes from diseased birds had a reduced influx of calcium (or release for intracellular stores) following stimulation. These data clearly reflect a unique defect in T cell activation associated with avian scleroderma. Analysis of chicken CD3, CD4 and CD8 expression revealed a 39% decrease in peripheral blood CD4+ cells in scleroderma birds, although this decrease was not sufficient to explain the 80-90% decrease observed in proliferation assays and calcium influx. Our data support the hypothesis that avian scleroderma is mediated via abnormal function of lymphocyte co-stimulatory molecules or intracellular calcium regulators.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0896-8411
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
5
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
261-76
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:1388634-Animals,
pubmed-meshheading:1388634-Antigens, Differentiation, T-Lymphocyte,
pubmed-meshheading:1388634-Autoimmune Diseases,
pubmed-meshheading:1388634-Calcium,
pubmed-meshheading:1388634-Chickens,
pubmed-meshheading:1388634-Disease Models, Animal,
pubmed-meshheading:1388634-Genes, MHC Class I,
pubmed-meshheading:1388634-Leukocyte Count,
pubmed-meshheading:1388634-Lymphocyte Activation,
pubmed-meshheading:1388634-Mitogens,
pubmed-meshheading:1388634-Poultry Diseases,
pubmed-meshheading:1388634-Scleroderma, Systemic,
pubmed-meshheading:1388634-T-Lymphocyte Subsets
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pubmed:year |
1992
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pubmed:articleTitle |
Avian scleroderma: evidence for qualitative and quantitative T cell defects.
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pubmed:affiliation |
Department of Internal Medicine, University of California, Davis 95616.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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